Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 24-year-old woman developed bilateral blindness after recovery from coma secondary to acute intermittent porphyria. Gradual return of vision in the right eye with a permanent unilateral visual field defect and optic atrophy followed. We believe the pathophysiologic mechanism was spasm of the vessels supplying the optic disk leading to ischemia and infarction of the optic nerve.
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PMID:Optic atrophy in acute intermittent porphyria. 43 76

A 10-year-old girl developed bilateral blindness and partial third nerve paresis immediately following a closed head injury. Bilateral optic atrophy developed subsequently. This is the first report of an association between second and third nerve injuries after minor head trauma in the absence of a preexisting lesion. The pathophysiology of indirect injury to the optic nerve under these circumstances is uncertain, but the lesions in this patient seemed to be due to ischemia.
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PMID:Total blindness after trivial frontal head trauma: bilateral indirect optic nerve injury. 57 Jun 62

Drainage-retinotomies and relaxing retinectomies are helpful techniques in extreme vitreoretinal surgery. They have become established as a surgical instrument, but their possible pathophysiologic effects on the retina, pigment epithelium and choroid have not been investigated as yet. 30 Patients with retinotomies or retinectomies after vitrectomy with silicone oil filling for advanced proliferative vitreoretinopathy were studied angiographically. Fluorescein angiographic findings revealed 1. a predominant effect of endophotocoagulation in the area of the retinotomy/retinectomy with occlusion of the choriocapillaris and hyperpigmentation and window effects of the retinal pigment epithelium, but sometimes there was a localized traction effect with retinal and choroidal folds, 2. that retinal perfusion is unaffected in untreated and coagulated areas without evidence for a breakdown of the blood-retina-barrier or retinal ischemia, 3. an intact blood-retinal-barrier in areas of uncovered retinal pigment epithelium, 4. no evidence for significant reproliferations in the areas of retinotomies and retinectomies, 5. choroidal neovascular membranes which may occur postoperatively at the retinotomy site probably as a complication for intraoperative injury of Bruch's membrane, 6. a cystoid macular edema, an optic atrophy, pigment-fallout, depigmented tracks and choroidal folds as unspecific findings post retinal detachment surgery. The angiographic data support the clinical impression, that retinotomies and retinectomies performed in otherwise untreatable cases cause no significant damage in the attached retina.
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PMID:[Fluorescein angiography findings after retinotomy and retinectomy]. 175 69

Bilateral blindness resulting from optic atrophy is an unusual complication following shock and cardio-respiratory arrest. This report describes a patient with acute respiratory failure due to pneumococcal pneumonia being treated with very high levels of positive end expiratory pressure who developed bilateral blindness following cardiac arrest. This unfortunate complication most likely resulted from increased intraocular pressure and low systemic perfusion pressure synergistically causing ischemia of the optic nerves.
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PMID:Bilateral optic atrophy after cardiac arrest in a patient with acute respiratory failure on positive pressure ventilation. 283 2

Two adult diabetic patients with chronic asymptomatic optic neuropathy attributed to an ischemic etiology are reported. In one case the typical syndrome of ischemic optic neuropathy occurred in one eye, while the fellow eye had asymptomatic hyperemic optic disc edema that persisted for 6 months without optic atrophy. A minor visual field defect initially detected in that eye resolved spontaneously in 1 month. In the second case, a recent onset, middle-aged diabetic developed bilateral optic neuropathy and optic disc edema that persisted for 12 months, with minimal signs of visual dysfunction. Axoplasmic transport blockage from low-grade ischemia to the optic nerve may cause acute or chronic optic disc edema with minimal or no visual symptoms.
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PMID:Chronic asymptomatic ischemic optic neuropathy. A report of two cases in adults with diabetes mellitus. 296 25

The amplitude of the second harmonic of the focal electroretinogram (ERG) in response to either modulation of the luminance of the uniform-field or the spatial contrast of a patterned field (pattern-reversal ERG) was measured in a group of normal subjects as well as in patients with two different types of unilateral dysfunctions, namely optic atrophy or temporary retinal ischemia. Such patients had a reduced visual acuity in their affected eyes but normal full-field flicker (20 Hz) ERG. In normal eyes, for the same stimulation area and modulation depth, the second harmonic of the uniform-field response is smaller (mean value 62%) than that of the optimal pattern (around 1.5 cycles/degree). The results on patients show that the second harmonic of the pattern response, but not that of the uniform-field response, is reduced in cases of optic atrophy secondary to trauma or optic neuritis. This result suggests generators different, at least in part, for the second harmonic evoked by modulation of either luminance or spatial contrast. By contrast, both responses are reduced in cases of temporary retinal ischemia. These findings are discussed in light of the recent literature on the origin of the pattern ERG. The possible clinical applications of the technique are outlined.
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PMID:Non-linearities in the focal ERG evoked by pattern and uniform-field stimulation. Their variation in retinal and optic nerve dysfunction. 361 May 49

The authors present five cases of severe retinal ischemia associated with gentamicin injection. In three of the cases massive doses of gentamicin were erroneously injected into the eye; in two of the cases the authors presume that gentamicin toxicity occurred. The sequence of clinical findings was similar in all five cases. The prominent findings included early superficial and intraretinal hemorrhages, opaque and edematous retina, cotton-wool infarcts, arteriolar narrowing, and venous beading. Fluorescein angiography revealed severe retinal vascular nonperfusion. Chronic findings included rubeosis irides, neovascular glaucoma, retinal pigmentary degeneration, and optic atrophy. Of the documented cases of massive intraocular gentamicin injection, two patients had no light perception (NLP) vision and one had bare light perception. Of the two cases of presumed gentamicin toxicity, one had 20/400 vision and one had count fingers vision. Strict precautions are necessary to prevent the catastrophic events resulting from inadvertent gentamicin injection; such precautions should include precise labeling of all injectable solutions on the surgical field, waiting to draw up injectable antibiotics until the time they are needed, and drawing up injectable antibiotics under direct physician observation. All intravitreal injections should be performed slowly, in the anterior vitreous, with the needle bevel up.
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PMID:Retinal toxicity secondary to intraocular gentamicin injection. 376 30

Accelerated renovascular hypertension produces optic nerve changes ranging from optic disc edema to optic atrophy. To elucidate the pathogenesis of hypertensive optic neuropathy, the optic nerves from 12 monkeys (23 eyes) with accelerated renovascular systemic hypertension were studied by electron and light microscopy. Within 21 months, the animals demonstrated the entire spectrum of pathologic changes. In the optic nerves with optic disc edema, the prelaminar optic nerve exhibited vasoconstriction with subsequent axonal hydropic swelling, axolemma disruption, and glial swelling. In retrolaminar myelinated optic nerve, vasoconstriction was more severe, with endothelial swelling and pericytic degeneration resulting in intramyelinic vacuoles and glial swelling. Optic disc edema appeared to result from axonal hydropic swelling secondary to ischemic infarct, followed by loss of axons and gliosis in the prelaminar optic nerve. The retrolaminar myelinated nerve showed prominent microglial reaction and eventual atrophy of axons and glia. Ischemia seemed to play a major role in hypertensive optic neuropathy, which represents anterior ischemic optic neuropathy.
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PMID:Fundus lesions in malignant hypertension. II. A pathologic study of experimental hypertensive optic neuropathy. 402 51

Two unusual cases of ocular toxoplasmosis are presented. A 24 year old woman developed retinal and optic nerve neovascularization in conjunction with acute ocular toxoplasmosis. The neovascularization regressed with resolution of the inflammation. The possibility of retinal ischemia or inflammation alone as an etiology are discussed. A 19 year old woman developed optic nerve edema and a marked decrease in vision associated with a nasal toxoplasma lesion and a macular star. With resolution of the process, optic atrophy developed but visual acuity returned to normal. Optic nerve edema and atrophy were felt to result from diffuse inflammation, but not from focal involvement in the nerve itself with the organism.
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PMID:Unusual presentation of acute ocular toxoplasmosis. 616 56

Iatrogenic pathology of the optic nerve is examined according to a framework which distinguishes direct and indirect effects on the optic nerve. Direct effects due to toxic drugs should be suspected when unexplained, usually bilateral loss of visual acuity occurs. The 3 clinical stages of classical optic toxic neuropathy are 1) anomalies of color vision, 2) loss of visual acuity and narrowing field of vision, and 3) papillary palor corresponding to irreversible optic atrophy. Usually only the 1st stages are reversible, but the reversibility may be incomplete. The list of drugs which can cause such effects is lengthy and includes antiinfectious drugs such as sulfamides and derivatives of hydroxyquinoleins, chloramphenicol especially when used to treat cystic fibrosis of the pancreas in children, the antituberculins ethambutol in high doses and isoniazide, which occasion particular risks when combined; antiparasitics such as quinine and its derivatives chloroquine and hydroxychloroquine, which cause optic neuropathy through their effect on the retina; arsenic pentavalents such as tryparsamide, quinacrine, trecator and mystatin; drugs affecting the central nervous system such as monoamineoxydase inhibitors, laroxyl, phenothiazine and the barbituates; anticonvulsants such as phenytoin; antimitotics such as vincristine; digitalics, disulfiram; penicillamines, and pexid. The action of lasers on the optic nerve can have a similar effect. The optic nerve may be indirectly damaged during surgical procedures leading to hypotonia, acute ischemia of the head of the optic nerve or embolic accident after a local or regional injection. Damage may also be caused by radiotherapy of intracranial tumors and certain drugs which cause isolated papillary edema or edema associated with headaches, such as Tetracycline, large doses of vitamin A or D, corticoids, and oral contraceptive (OC) pills, which may cause papillary edema through cerebral pseudo-tumors that regress with discontinuation of treatment. This condition has been observed in women with uncontrolled hyperlipidemia. It is probable that an alteration ofaxonal transport is at the basis of the neuropathic mechanisms. The 1st step in therapy is the suppression of the toxin, or at least its discontinuation. Some success has been obtained with vitamin B therapy, corticotherapy, zinc, or isaxonine, depending on the specific condition.
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PMID:[Iatrogenic pathology of the optic nerve]. 676 92


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